Journals / Turkish Journal of Hematology / 2011 / Cilt: 28 - Sayı: 3

Çocukluk çağı idiopatik trombositopenik purpura'da TNF-α-308G/A ve TGF-β1-915G/C polimorfizmlerinin rolü

The role of tumor necrosis factor-alpha -308 G/A and transforming growth factor-beta 1 -915 G/C polymorphisms in childhood idiopathic thrombocytopenic purpura

Pages
170–175
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion: The frequency of TNF-α -308 G/A and TGF-β1 -915 G/C polymorphisms did not differ between pediatric ITP patients and healthy controls, and these polymorphisms were not associated with susceptibility to the development and clinical progression of the disease.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: To increase our understanding of the etiology of idiopathic thrombocytopenic purpura (ITP) some cytokine gene polymorphisms were analyzed for susceptibility to the disease.
📊
Key Findings & Data:The aim of this study was to investigate the role of tumor necrosis factor-alpha (TNF-α) -308 G/A and transforming growth factor-beta 1 (TGF-β1) –915 G/C polymorphisms in the development and clinical progression of childhood ITP Materials and Methods: In all, 50 pediatric patients with ITP (25 with acute ITP and 25 with chronic ITP) and 48 healthy controls were investigated via LightCycler® PCR analysis for TNF-α -308 G/A and TGF-β1 -915 G/C polymorphisms.
💡
Conclusion & Impact:Conclusion: The frequency of TNF-α -308 G/A and TGF-β1 -915 G/C polymorphisms did not differ between pediatric ITP patients and healthy controls, and these polymorphisms were not associated with susceptibility to the development and clinical progression of the disease.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objective: To increase our understanding of the etiology of idiopathic thrombocytopenic purpura (ITP) some cytokine gene polymorphisms were analyzed for susceptibility to the disease. The aim of this study was to investigate the role of tumor necrosis factor-alpha (TNF-α) -308 G/A and transforming growth factor-beta 1 (TGF-β1) –915 G/C polymorphisms in the development and clinical progression of childhood ITP Materials and Methods: In all, 50 pediatric patients with ITP (25 with acute ITP and 25 with chronic ITP) and 48 healthy controls were investigated via LightCycler® PCR analysis for TNF-α -308 G/A and TGF-β1 -915 G/C polymorphisms. Results: The frequency of TNF-α -308 G/A polymorphism was 20%, 16%, and 22.9% in the acute ITP patients, chronic ITP patients, and controls, respectively (p>0.05). The frequency of TGF-β1 -915 G/C polymorphism was 16%, 8%, and 8.3% in the acute ITP patients, chronic ITP patients, and controls, respectively (p>0.05). The risk of developing ITP and clinical progression were not associated with TNF-α -308 G/A (OR: 0.738, 95% CI: 0.275-1.981, and OR: 0.762, 95% CI: 0.179-3.249) or TGF-β1 -915 G/C (OR: 1.5, 95% CI: 0.396-5.685, and OR: 0.457, 95% CI: 0.076-2.755) polymorphisms. Conclusion: The frequency of TNF-α -308 G/A and TGF-β1 -915 G/C polymorphisms did not differ between pediatric ITP patients and healthy controls, and these polymorphisms were not associated with susceptibility to the development and clinical progression of the disease.

Özet

Amaç: İdiopatik trombositopenik purpura (ITP)’nın etyolojisini anlayabilmek için, hastalığa yatkınlık üzerinde bazı sitokin gen polimorfizmleri incelenmiştir. Bu çalışmanın amacı çocukluk çağı ITP’sinin gelişimi ve klinik seyrinde tümör nekrozis faktör-alfa (TNF-α) –308G/A ve transforming growth faktör- beta1 (TGF-β1) -915G/C polimorfizmlerinin rolünü araştırmaktır. Yöntem ve Gereçler: Elli ITP’li çocuk hasta (25 akut ITP 25 kronik ITP) ve 48 sağlıklı kontrol TNF-α– 308G/A ve TGF-β1–915G/C polimorfizmleri için Light Cycler PCR analizi ile araştırıldı. Bulgular: Akut ITP kronik ITP ve kontrollerde TNF-α–308G/A polimorfizm sıklığı sırasıyla %20, %16 ve %22.9 (p>0.05), ve TGF-β1–915G/C polimorfizm sıklığı sırasıyla %16, %8 ve %8.3 (p>0.05) idi. ITP gelişim riski ve klinik seyri ile TNF-α–308G/A (OR: 0.738, %95 Cl: 0.275-1.981 ve OR: 0.762, %95 Cl: 0.179-3.249) ve TGF-β1–915G/C (OR: 1.5, %95 Cl: 0.396-5.685 ve OR: 0.457, %95 Cl: 0.076-2.755) polimorfizmleri arasında ilişki bulunamadı. Sonuç: Bu sonuçlar, çocukluk çağı ITP hastalarında TNF-α–308G/A ve TGF-β1–915G/C polimorfizmlerinin sıklığının sağlıklılardan farklı olmadığını göstermiş olup, bu polimorfizmlerin ITP gelişimi ve hastalığın klinik seyri için risk oluşturmadığını düşündürmektedir.

🔖

Cite This Article

OKULU, E., İLERİ, D. T., KOŞAN, V. Ç., AZIK, F. M., EĞİN, Y., UYSAL, Z., AKAR, N. (2011). Çocukluk çağı idiopatik trombositopenik purpura'da TNF-α-308G/A ve TGF-β1-915G/C polimorfizmlerinin rolü. Turkish Journal of Hematology, Cilt: 28 - Sayı: 3, 170–175. https://ajindex.com/articles/413343

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (13)

  1. Nugent DJ. Childhood immune thrombocytopenic pur- pura. Blood Reviews 2002;16:27-9.
  2. Blanchette V, Bolton-Maggs P. Childhood immune thrombocytopenic purpura: Diagnosis and manage- ment. Hematol Oncol Clin N Am 2010;24:249-73.
  3. Yaprak I, Atabay B, Durak I, Turker M, Oniz H, Ozer EA. Variant clinical courses in children with immune throm- bocytopenic purpura: Sixteen year experience of a sin- gle medical center. Turk J Hematol 2010;27:147-55. Andersson J. Cytokines in idiopathic thrombocytope- nic purpura (ITP). Acta Paediatr Suppl 1998;424:61-4.
  4. Bidwell JL, Wood NA, Morse HR, Olomolaiye OO, Keen LJ, Laundy GJ. Human cytokine gene nucleotide sequence aligments: supplement 1. Eur J Immunogenet 1999;26:135-223.
  5. Wilson AG, Symons JA, McDowell TL, McDevitt HO, Duff GW. Effects of a polymorphism in the human tumor necrosis factor α promoter on transcriptional activation. Proc Natl Acad Sci USA 1997;94:3195-9.
  6. Foster CB, Zhu S, Erichsen HC, Lehrnbecher T, Hart ES, Choi E, Stein S, Smith MW, Steinberg SM, Imbach P Künhe T, Chanock SJ; Early Chronic ITP Study Group. Polymorphisms in inflammatory cytokines and Fcγ recep- tors in childhood chronic immune thrombocytopenic purpura: a pilot study. Br J Haematol 2001;113:596-9.
  7. Chang WW, Su H, He L, Zhao KF, Wu JL, Xu ZW. Association between transforming growth factor-β1 T869C polymorphism and rheumatoid arthritis: a meta- analysis. Rheumatology 2010;49:652-6.
  8. Blobe GC, Schieman WP Lodish HF. Role of transform- ing growth factor-β in human disease. N Eng J Med 2000;18:1350-8.
  9. Letterio JJ, Roberts AB. Regulation of immune respons- es by TGF-β. Annu Rev Immunol 1998;16:137-61.
  10. Atabay B, Oren H, Irken G, Kizildağ S, Tunali S, Türker M, Yilmaz S. Role of transforming growth factor-β1 gene polymorphisms in childhood idiopathic thrombo- cytopenic purpura. J Pediatr Hematol Oncol 2003;25:885-9.
  11. Akar N, Hasipek M. Tumour necrosis factor-alpha gene polymorphism (-308 G-A) in Turkish pediatric throm- bosis patients. Turk J Hematol 2002;19:39-41.
  12. George JN, Woolf SH, Raskob GE, Wasser JS, Aledort LM, Ballem PJ, Blanchette VS, Bussel JB, Cines DB, Kelton JG, Lichtin AE, McMillan R, Okerbloom JA, Regan DH, Warrier I. Idıopathic thrombocytopenic pur- pura: A practice guideline developed by explicit meth- ods fort he American Society of Hematology. Blood 1996;88:3-40. Richardson B. Primer; Epigenetics of autoimmunity. Nat Clin Pract Rheumatol 2007;3:521-7.
  13. Castro V, Oliveira GB, Origa AF, Annichino-Bizzacchi JM, Arruda VR. The human plate